Background: The morbidity and mortality associated with tobacco smoking is well established.
Nicotine is the addictive component of tobacco. Nicotine, through the non-neuronal α7nicotinic
receptor, induces cell proliferation, neo-angiogenesis, epithelial to mesenchymal transition, and inhibits
Objective: To understand the genetic, molecular and cellular biology of addiction, chronic obstructive
pulmonary disease and lung cancer.
Methods: The search for papers to be included in the review was performed during the months of July-
September 2018 in the following databases: PubMed (http://www.ncbi.nlm.nih.gov), Scopus
(http://www.scopus.com), EMBASE (http://www.elsevier.com/online-tools/embase), and ISI Web of
Knowledge (http://apps.webofknowledge.com/). The following searching terms: “nicotine”, “nicotinic
receptor”, and “addiction” or “COPD” or “lung cancer” were used.
Patents were retrieved in clinicaltrials.gov (https://clinicaltrials.gov/). All papers written in English
were evaluated. The reference list of retrieved articles was also reviewed to identify other eligible
studies that were not indexed by the above-mentioned databases.
New experimental data on the ability of nicotine to promote transformation of human bronchial epithelial
cells, exposed for one hour to Benzo[a]pyrene-7,8-diol-9-10-epoxide, are reported.
Results: Nicotinic receptors variants and nicotinic receptors upregulation are involved in addiction,
chronic obstructive pulmonary disease and/or lung cancer. Nicotine through α7nicotinic receptor upregulation
induces complete bronchial epithelial cells transformation.
Conclusion: Genetic studies highlight the involvement of nicotinic receptors variants in addiction,
chronic obstructive pulmonary disease and/or lung cancer. A future important step will be to translate
these genetic findings to clinical practice. Interventions able to help smoking cessation in nicotine
dependence subjects, under patent, are reported.